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[Display omitted] • NiFeRu/C and Ru, Fe-Ni 5 P 4 /C nanofibers as complementary electrocatalyst toward water splitting were synthesized. • The electrolytic cell based NiFeRu/C||Ru, Fe-Ni 5 P 4 /C presents outstanding water splitting activity owing to their complementary activity. • NiFeRu/C||Ru, Fe-Ni 5 P 4 /C requires voltage of 1.569, 1.744 and 1.872 V to achieve 100, 500 and 1000 mA cm−2, respectively. • NiFeRu/C||Ru, Fe-Ni 5 P 4 /C can work stability at 500 mA cm−2 for 100 h. Designing and fabricating highly competent and inexpensive electrocatalysts are highly desirable for application in electrocatalytic water splitting. In this study, we synthesized NiFeRu/C nanofibers and Ru, Fe dual-doped Ni 5 P 4 (Ru, Fe-Ni 5 P 4)/C nanofibers as complementary electrocatalysts for overall water splitting through electrospinning, carbonization, and phosphorization treatment, respectively. The NiFeRu/C nanofibers and Ru, Fe-Ni 5 P 4 /C nanofibers showed high hydrogen evolution reaction and oxygen evolution reaction activity, respectively, due to the presence of numerous exposed active sites and optimized adsorption capacity for the reaction intermediates contributed by the synergistic interaction among different metal components in the electrocatalysts. Hence, the assembled asymmetrical electrolytic cell effectively promoted overall water splitting, requiring a voltage of 1.569, 1.744, and 1.872 V to achieve a current density of 100, 500, and 1,000 mA cm−2, respectively, and it was better than Pt/C||IrO 2. Additionally, the electrolytic cell could work at 500 mA cm−2 for 100 h without any noticeable deterioration in activity, which indicated that it was durable at high current density. In this study, we described a novel method for designing highly efficient electrocatalysts for overall water splitting. [ABSTRACT FROM AUTHOR]

[Display omitted] • NiMo solid-solution alloy porous nanofibers have been fabricated. • Alloying Ni with Mo can significantly enhance the HER activity. • NiMo solid-solution alloy porous nanofibers require a low overpotential of 69 mV at 100 mA cm−2. • NiMo solid-solution alloy porous nanofibers can work stably at 100 mA cm−2 for 60 h. Developing a high-efficiency hydrogen evolution reaction (HER) electrocatalyst for the large-scale production of hydrogen is essential but challenging. In this study, we used NiMo solid-solution alloy porous nanofibers to develop a robust HER electrocatalyst through electrospinning, oxidization, and high-temperature reduction treatment. In 1 M KOH electrolyte, the fabricated NiMo solid-solution alloy porous nanofibers exhibited higher HER activity than Ni nanofibers, which required a low overpotential of 69, 208, and 300 mV at 100, 500, and 1000 mA cm−2, respectively, and had outstanding durability at 100 mA cm−2 over 60 h. We developed a promising candidate for a high-efficiency HER electrocatalyst, and our findings provided valuable information for fabricating highly robust alloy-based electrocatalysts. [ABSTRACT FROM AUTHOR]

Reduction in L-type Ca2+ current (I Ca,L) density is a hallmark of the electrical remodeling in atrial fibrillation (AF). The expression of miR-155, whose predicted target gene is the α1c subunit of the calcium channel (CACNA1C), was upregulated in atrial cardiomyocytes (aCMs) from patients with paroxysmal AF.The study is to determine miR-155 could target the gene expression of I Ca,L and contribute to electrical remodeling in AF. The expression of miR-155 and CACNA1C was assessed in aCMs from patients with paroxysmal AF and healthy control. I Ca,L properties were observed after miR-155 transfection in human induced pluripotent stem cell derived atrial cardiomyocytes (hiPSC-aCMs). Furthermore, an miR-155 transgene (Tg) and knock-out (KO) mouse model was generated to determine whether miR-155 was involved in I Ca,L -related electrical remodeling in AF by targeting CACNA1C. The expression level of miR-155 was increased, while the expression level of CACNA1C reduced in the aCMs of patients with AF. miR-155 transfection in hiPSC-aCMs produced changes in I Ca,L properties qualitatively similar to those produced by AF. miR-155/Tg mice developed a shortened action potential duration and increased vulnerability to AF, which was associated with decreased I Ca,L and attenuated by an miR-155 inhibitor. Finally, the genetic inhibition of miR-155 prevented AF induction in miR-155/KO mice with no changes in I Ca,L properties. The increased miR-155 expression in aCMs was sufficient for the reduction in the density of I Ca,L and the underlying electronic remodeling. The inhibition of miR-155 prevented I Ca,L -related electric remodeling in AF and might constitute a novel anti-AF approach targeting electrical remodeling. [Display omitted] • The reduction in the density of I Ca,L is a hallmark of remodeling in AF. • Expression of miR-155 increased in cardiomyocytes from patients with AF. • Increased miR-155 expression is sufficient for the reduction of I Ca,L. • Inhibition of miR-155 prevented I Ca,L -related electric remodeling in AF. • miR-155 is a novel therapy target for I Ca,L related electrical remodeling. [ABSTRACT FROM AUTHOR]

• M-C-FDU-15(x) (M = Na, K, Rb and Cs) was prepared using in-situ process by alkali modified C-FDU-15. • M-C-FDU-15(0.01) have different NO + O 2 adsorption properties, and Na-C-FDU-15(0.02) exhibit high efficiency. • Compared with C-FDU-15, the specific surface area and pore volume of M-C-FDU-15(0,01) (M = Na and K) enhanced, while M-C-FDU-15(0.01) (M = Rb and Cs) dropped. • Proper pore volume, basic sites and the smaller ionic radius of alkali-metal ions of M-C-FDU-15(x) are vital factors on NO + O 2 adsorption. • The adsorption of NO + O 2 by M-C-FDU-15(x) is mainly chemisorption which produces nitrites (NO 2 −) and nitrates (NO 3 −) in this progress. The alkali metal (M = Na, K, Rb, and Cs)-modified C-FDU-15 (M-C-FDU-15(x); x was the M/C-FDU-15 M ratio, and equal to 0.01–0.03) samples were prepared through an in situ process, and characterized by means of the TG, XRD, TEM, EDS, N 2 adsorption–desorption, O 2 -TPD, and CO 2 -TPD techniques. The (NO + O 2) adsorption mechanism was investigated using the (NO + O 2)-TPD and DRIFTS techniques. The results show that the sequence of (NO + O 2) adsorption performance was Na-C-FDU-15(0.01) (104.1 mg/g) > K-C-FDU-15(0.01) (92.4 mg/g) > C-FDU-15 (76.2 mg/g) > Rb-C-FDU-15(0.01) (65.1 mg/g) > Cs-C-FDU-15(0.01) (62.3 mg/g). The alkali metal was uniformly distributed in C-FDU-15 and its doping enhanced the amount of the basic sites in the sample. Moreover, the optimal Na/C-FDU-15 M ratio was 0.02. (NO + O 2) were chemically adsorbed mainly in the forms of nitrite (NO 2 −) and nitrate (NO 3 −) on M-C-FDU-15(x). A more amount of NO was converted to nitrate than to nitrite. There were three key factors of enhancing the (NO + O 2) adsorption capacity of C-FDU-15 due to alkali metal doping: the first factor was the increasing of surface area and pore volume of the sample, the second one was the enhancement in amount of the active sites in the sample, and the third one was the smaller alkali metal ionic radius in the sample. [ABSTRACT FROM AUTHOR]

Aiming at the problem of unclear or missing human object interaction behavior objects in complex background, we propose a human object interaction detection algorithm based on feature optimization and key human-object enhancement. In order to solve the problem of missing human behavior objects, we propose Feature Optimized Faster Region Convolutional Neural Network (FOFR-CNN). FOFR-CNN is an object detection network optimized by multi-scale feature optimization algorithm, taking into account both image semantics and image structure. In order to reduce the interference of complex background, we propose a Key Human-Object Enhancement Network. The network uses an instance-based method to enhance the features of interactive objects. In order to enrich the interaction information, we use the graph convolutional network. Experimental results on HICO-DET, V-COCO and HOI-A datasets show that the proposed algorithm has significantly improved accuracy and multi-scale object detection ability compared with other human object interaction algorithms. [ABSTRACT FROM AUTHOR]

Idiopathic nephrotic syndrome (INS) is a common renal disease characterized by disruption of the glomerular filtration barrier. In a previous study, we screened and identified podocyte autoantibodies in nephrotic syndrome patients and proposed the concept of autoimmune podocytopathy. However, circulating podocyte autoantibodies cannot reach podocytes unless glomerular endothelial cells have been damaged. Therefore, we speculate that INS patients may also have autoantibodies against vascular endothelial cells. Sera from INS patients were used as primary antibodies to screen and identify endothelial autoantibodies by hybridization with vascular endothelial cell proteins separated by two-dimensional electrophoresis. The clinical application value and pathogenicity of these autoantibodies were further verified by clinical study and in vivo and in vitro experiments. Nine kinds of autoantibodies against vascular endothelial cells were screened in patients with INS, which can cause endothelial cell damage. In addition, 89% of these patients were positive for at least one autoantibody. The two-hit hypothesis of Autoimmune Podocytopathies: the pathogenic process of INS is first initiated by damage caused by pathogenic factors such as antiantibodies to glomerular endothelial cells, and subsequently, podocytes are exposed to those causative factors that lead to the occurrence of disease. [Display omitted] [ABSTRACT FROM AUTHOR]

Academia and industry have strengthened each other under the guidelines of regulatory institutions to contribute theoretical knowledge and practical solutions for society, which can be presented in a combination of publishing research and filing patents. In the case of municipal solid waste management (MSWM), a great transformation from a linear to a circular view has been in process. In this study, we investigated the role of the United Nations Sustainable Development Goals (SDGs) in MSWM-related development and transformation. The authors examined the contributions of academic and industrial spheres to MSWM in the past 70 years by examining Web of Science's Core Collection and Derwent Innovations Index. The results showed that SDGs not only accelerated the research on MSWM but also pulled MSWM-related knowledge and innovation to new fronts that focus on sustainable and circular methods. Based on the current findings, we derived implications for academia, industry, and policymakers. • Academia and industry are playing vital role in addressing MSWM-related development. • Implementing SDG-17 is required between developed and developing regions. • Hard (i.e. sustainability assessment) and soft (i.e. financial risk) are most crucial issues. [ABSTRACT FROM AUTHOR]

Kawasaki disease (KD) has become the most common cause of acquired heart disease in children and is also a risk factor for ischemic heart disease in adults. However, Kawasaki disease lacks specific laboratory diagnostic indices. Thus, this study analyzed the T cell activation profiles of Kawasaki disease and assessed their value in the diagnosis of Kawasaki disease and the prediction of intravenous immunoglobulin (IVIG) sensitivity. We analyzed human leukocyte antigen-DR (HLA-DR), CD69 and CD25 expression on peripheral blood CD4 + and CD8 + T cells during the acute phase of KD. We compared the percentages of HLA-DR +/CD69 +/CD25 + T cells in the CD4 + and CD8 + T cell populations of IVIG-effective and IVIG-resistant groups. Receiver operating characteristic curves were used to assess the diagnostic value of the above parameters. The median percentage of CD8 + HLA-DR + T cells and the median ratio of CD8 + HLA-DR + T cells/CD8 + CD25 + T cells were significantly elevated in the patient group compared with those in the control group during the acute phase of KD. Regarding the diagnosis of Kawasaki disease, the area under the ROC curve was 0.939 for the percentage of CD8 + HLA-DR + T cells. There was a significant difference in the ratio of CD8 + HLA-DR + T cells/CD8 + CD69 + T cells between IVIG-resistant patients and IVIG-sensitive patients. Regarding IVIG sensitivity, the area under the ROC curve was 0.795 for it. Excessive CD8 + T cell activation, as well as an imbalance between CD8 + T cell activation and inhibition, underlies the pathogenesis of Kawasaki disease. The percentage of CD8 + HLA-DR + T cells may be used as an index to diagnose Kawasaki disease. IVIG inhibits CD8 + T cell activation, but excessive CD8 + T cell activation may cause IVIG resistance. The ratio of CD8 + HLA-DR + T cells/CD8 + CD69 + T cells may be used as a predictor of IVIG sensitivity. [ABSTRACT FROM AUTHOR]

Abstract: Our laboratory has reported earlier that in leukocytes, phospholipase D2 (PLD2) is under control of Janus kinase 3 (JAK3), which mediates chemotaxis. Investigating JAK3 in cancer cells led to an important discovery as exponentially growing MDA-MB-231 human breast cancer cells, which are highly proliferative and metastatic, did not substantially use JAK3 to activate PLD2. However, in 2-h or 16-h starved cell cultures, JAK3 switches to a PLD2-enhancing role, consistent with the needs of those cells to enter a “survival state” that relies on an increase in PLD2 activity to withstand serum deprivation. Using a small-molecule tyrosine kinase inhibitor, the flavonoid 4'',5,7-trihydroxyflavone (apigenin), as well as RNA silencing, we found that the invasive phenotype of MDA-MB-231 cells is mediated by PLD2 under direct regulation of both JAK3 and the tyrosine kinase, epidermal growth factor receptor (EGFR). Furthermore, serum-deprived cells in culture show an upregulated EGFR/JAK3/PLD2-PA system and are especially sensitive to a combination of JAK3 and PLD2 enzymatic activity inhibitors (30nM apigenin and 300nM 5-fluoro-2-indolyl des-chlorohalopemide (FIPI), respectively). Thus, a multi-layered activation of cell invasion by two kinases (EGFR and JAK3) and a phospholipase (PLD2) provides regulatory flexibility and maximizes the aggressively invasive power of MDA-MB-231 breast cancer cells. This is especially important in the absence of growth factors in serum, coincidental with migration of these cells to new locations. [Copyright &y& Elsevier]

Kazal-type inhibitors (KPIs) play important roles in many biological and physiological processes, such as blood clotting, the immune response and reproduction. In the present study, two male reproductive tract KPIs, termed Man-KPI and Ers-KPI, were identified in Macrobrachium nipponense and Eriocheir sinensis, respectively. The inhibitory activities of recombinant Man-KPI and Ers-KPI against chymotrypsin, elastase, trypsin and thrombin were determined. The results showed that both of them strongly inhibit chymotrypsin and elastase. Kinetic studies were performed to elucidate their inhibition mechanism. Furthermore, individual domains were also expressed to learn further which domain contributes to the inhibitory activities of intact KPIs. Only Man-KPI_domain3 is active in the inhibition of chymotrypsin and elastase. Meanwhile, Ers-KPI_domain2 and 3 are responsible for inhibition of chymotrypsin, and Ers-KPI_domains2, 3 and 4 are responsible for the inhibition of elastase. Meanwhile, the inhibitory activities of these two KPIs toward Macrobrachium rosenbergii, M. nipponense and E. sinensis sperm were compared with that of the Kazal-type peptidase inhibitor (MRPINK) characterized from the M. rosenbergii reproductive tract in a previous study. The results demonstrated that KPIs can completely inhibit the gelatinolytic activities of sperm proteases from their own species, while different levels of cross-inhibition were observed between KPI and proteases from different species. These results may provide new perspective to further clarify the mechanism of KPI-proteases interaction in the male reproductive system. [ABSTRACT FROM AUTHOR]

Abstract: We propose and analyze theoretically a method to compensate gain-narrowing effect by using the spectral shaping technology based on superstructure fiber Bragg grating (SSFBG) in high-power Nd:glass chirped pulse amplification system. The target spectrum is firstly calculated from hundreds joules amplified chirped Gaussian or super-Gaussian pulse by an inverse engineering operation. A genetic algorithm is used to design the SSFBG and obtain the index modulation distribution of grating which can transform the initial seed pulse to the target spectrum. The numerically simulations show that the spectral narrowing effect of chirped pulse amplification will be reduced largely and the ideal pulse spectrum (Gaussian or super-Gaussian) is also obtained. It is believed that this proposed method will provide a theoretical direction for the following experiment. Moreover, it will also be useful and flexible for the spectral transform in other chirped pulse application areas. [Copyright &y& Elsevier]

Children with idiopathic nephrotic syndrome (INS) usually have podocyte injury, and recent studies suggest a B cell dysfunction in INS. Therefore, this study attempts to screen and identify the podocyte autoantibodies in patients. Two-dimensional electrophoresis and mass spectrometry were used to screen and identify the pathogenic podocyte autoantibodies in children with INS. The positive rate, expression pattern, and clinical correlation of these podocyte autoantibodies in children with INS were determined by clinical study. At least 66% of INS children have podocyte autoantibodies. Seven podocyte autoantibodies closely related to INS were screened and identified for the first time in this study. These podocyte autoantibodies are positively correlated with proteinuria, and its titer will decrease rapidly after effective treatment. In this study, a group of new disease subgroup-"autoimmune podocytes" were identified by podocyte autoantibodies. This paper used 2D electrophoresis combined with mass spectrometry to screen and identify podocyte autoantibodies specific to primary nephrotic syndrome. The protein microarray was used for clinical validation. Finally, seven podocytes autoantibodies specific to the serum of primary nephrotic syndrome were identified. These antibodies were positively correlated with urinary protein levels and efficacy. [Display omitted] [ABSTRACT FROM AUTHOR]

Recently, photocatalysis combined peroxydisulfate activation under visible light (PC-PDS/Vis) was developed as a promising technology for removing antibiotics in water. Herein, Mn doped FeOOH (Mn–FeOOH) nanoclusters were grown in-situ on the surface of graphitic carbon nitride nanosheets (CNNS) using a wet chemical method, which served as a visible-light-driven photocatalyst for peroxydisulfate (PDS) activation. Photovoltaic property characterizations revealed that Mn–FeOOH/CNNS owned superior light capture ability and carrier separation efficiency. According to DFT calculations, the synergistic effect between Mn and Fe species was proved to enhance the adsorption and activation of PDS. 99.7% of tetracycline (TC) was rapidly removed in 50 min in the PC-PDS/Vis system. In addition, Mn–FeOOH/CNNS exhibited high recycling stability with low iron leaching, attributed to the interaction between Mn–FeOOH clusters and carbon species. Quenching experiments and electron spin resonance (ESR) tests unveiled that •O 2 − played a significant role in TC removal, while •OH and SO 4 •- acted as additional roles contributing to the overall process. These findings given a new strategy for antibiotics degradation by photocatalysis, offering deeper insights for the advancement of sustainable and cutting-edge wastewater treatment technologies. [Display omitted] • Visible-light-driven photocatalysis coupled PDS system was used for water treatment. • Novel Mn–FeOOH/CNNS composite photocatalyst was synthesized by wet chemical method. • Tetracycline was degraded thorough synergistic photogenerated h+ and PDS activation. • Fe(III)/Fe(II) cycling was promoted by introducing Mn into FeOOH nanoclusters. [ABSTRACT FROM AUTHOR]

To improve the removal capacity of (NO ​+ ​O 2) effectively, the K-CMK-3(x) (KNO 3 : CMK-3 mass ratio (x) ​= ​10–20 ​wt%, in which CMK-3 is an abbreviation of the ordered mesoporous carbon) samples were prepared, and their physical properties and (NO ​+ ​O 2) adsorption performance were determined by means of analytical techniques, such as XRD, TEM, BET, TG, TPD, and DRIFTS. The ordered mesostructures were retained and specific surface areas and pore volumes of the K-CMK-3(x) samples increased after doping of K. Moreover, the doped K species were uniformly distributed on the surface of CMK-3, and K doping increased the amount of the basic sites in the sample. The structure and amount of the basic sites were the main factors influencing the (NO ​+ ​O 2) adsorption on the sample. The sequence in (NO ​+ ​O 2) adsorption performance was as follows: K-CMK-3(15) (143.8 ​mg/g) ​> ​K-CMK-3(20) (127.6 ​mg/g) ​> ​K-CMK-3(10) (103.6 ​mg/g) ​> ​CMK-3 (88.8 ​mg/g), with the K-CMK-3(15) sample possessing the best adsorption performance. There were two main adsorption pathways during the process of (NO ​+ ​O 2) adsorption: one pathway was the conversion of NO and O 2 to a large number of NO 2 , in which part of NO 2 was weakly adsorbed on the surface hydroxyl groups, and the other part of NO 2 was disproportionated to NO, NO 2 −, and NO 3 −; and the other pathway was first the direct oxidization of NO to NO 2 − by the oxygen functional groups in carbon and then some of the formed NO 2 − species were converted to NO 3 −. Image 1 • The K-CMK-3(15) exhibits a high (NO ​+ ​O 2) adsorption efficiency. • The structure of K-CMK-3(x) and more amount of basicity can improve adsorption (NO ​+ ​O 2). • The (NO ​+ ​O 2) adsorption on K-CMK-3(x) produces the NO 2 − and NO 3 − species. • Chemisorption dominates in the adsorption of (NO ​+ ​O 2) on K-CMK-3(15). [ABSTRACT FROM AUTHOR]

Several epidemiological studies reported that chronic arsenic exposure increased risk of prostate cancer. This study aimed to investigate whether chronic NaAsO 2 exposure elevates stemness and chemoresistance in prostate cancer cells. DU145 (wild-type p53) and PC-3 (p53-null) cells were exposed to NaAsO 2 (2 μmol/L) for 30 generations. IC50s to docetaxel and cisplatin were increased in NaAsO 2 -exposed DU145 and PC-3 cells. The number of tumor spheres was elevated in NaAsO 2 -exposed DU145 and PC-3 cells. Nanog, SOX-2 and ALDH1A1, three markers of cancer stemness, were upregulated in NaAsO 2 -exposed PC-3 spheres. Moreover, NaAsO 2 -exposed DU145 and PC-3 cells were arrested in G2/M phase. Histone H2AX phosphorylation on Ser139, an indicator for DNA double-strand break, was upregulated in NaAsO 2 -exposed DU145 and PC-3 cells. ATM phosphorylation on Ser1981, a key sensor of genotoxic stress, was rapidly elevated in NaAsO 2 -exposed DU145 cells. Phosphor-p53, a downstream molecule of ATM signaling, and p21, a direct target of p53, were upregulated in NaAsO 2 -exposed DU145 cells. Unexpectedly, p21 was also elevated in NaAsO 2 -exposed p53-null PC-3 cells. Antioxidant NAC alleviated NaAsO 2 -induced ATM phosphorylation, cell cycle arrest, and subsequent stemness enhancement and chemoresistance in both DU145 and PC-3 cells. These results suggest that ROS-mediated genotoxic stress is involved in NaAsO 2 -induced cell cycle arrest, stemness enhancement and chemoresistance of prostate cancer cells in a p53-independent manner. • Chronic NaAsO 2 promotes stemness and chemoresistance of prostate cancer cells. • Genotoxic stress is involved in NaAsO 2 -induced stemness of prostate cancer cells. • P53 is not necessary in NaAsO 2 -induced genotoxic stress of prostate cancer cells. • NAC attenuates stemness and chemoresistance in NaAsO 2 -exposed prostate cancer cells. [ABSTRACT FROM AUTHOR]

Effects of Al-pillaring and alkali metal (Li, Na, K and Cs) doping on CO 2 adsorption property of montmorillonite are investigated. Physicochemical properties of the materials are studied by means of X-ray diffraction and N 2 adsorption−desorption, and their CO 2 adsorption behaviors are studied using the thermogravimetic, CO 2 temperature-programmed desorption, and in situ diffuse reflectance fourier transform infrared spectroscopic techniques. Compared with montmorillonite, Al-pillaring improves its specific surface area (up to 242 ​m2/g) and pore structure. The results show that CO 2 adsorption capacity decreases in the sequence of 5 ​wt% Cs/Al-PILC > 5 ​wt% K/Al-PILC > 5 ​wt% Na/Al-PILC > 5 ​wt% Li/Al-PILC ​> ​Al-PILC ​> ​montmorillonite. Among all of the samples, the 5 ​wt% Cs/Al-PILC sample exhibits the highest adsorption capacity (2.325 ​mmol/g) at 50 ​°C. According to the adsorption kinetics analysis, CO 2 adsorption on montmorillonite is mainly chemical adsorption, so alkalinity of the adsorbent is improved by doping a proper amount of alkali metal. Meanwhile, the adsorbed CO 2 is stored in the form of bicarbonates and carbonates. Moreover, the montmorillonite adsorbents also have good regeneration properties. We believe that the results obtained in the present work provide more options for development of CO 2 adsorption adsorbents with high performance. Fig. Schematic adsorption mechanism of CO 2 on the samples. Image 1 • Montmorillonite adsorbents show good CO 2 low-temperature adsorption performance. • The main adsorption species on montmorillonite adsorbents are adsorbed bicarbonate and carbonate. • Montmorillonite adsorbents possess good regeneration efficiencies. [ABSTRACT FROM AUTHOR]

Evidence indicates that ferrostain-1 (Fer-1), a specific inhibitor of ferroptosis, could ameliorate cognitive dysfunction of rats with kainic acid (KA)-induced temporal lobe epilepsy (TLE) by suppressing ferroptosis processes. Recent studies suggest that P38 mitogen-activated protein kinase (MAPK) pathway could be mediated by ferroptosis processes. The activation of P38 MAPK results in cognitive impairment by suppressing the expression of synaptic plasticity-related proteins. However, it is unclear whether Fer-1 can mitigate cognitive impairment of rats with KA-induced TLE by inhibiting P38 MAPK activation. In the present study, treatment with Fer-1 blocked the activation of P38 MAPK, which resulted in an increased expression of synaptophysin (SYP) and postsynaptic density protein 95 (PSD-95) in the hippocampus of rats with KA-induced TLE, hence, ameliorating their cognitive impairment. Also, P38 MAPK activation in the hippocampus of the rats reduced the expression of both PSD-95 and SYP proteins. Treatment of the rats with SB203580, a P38 MAPK-specific inhibitor, prevented the activation of P38 MAPK, which resulted in an increase in SYP and PSD95 protein levels in the hippocampus. These results suggest that Fer-1 could mitigate the cognitive impairment by suppressing P38 MAPK activation thus restoring the expression of synaptic proteins. Ferroptosis processes might be involved in suppressing synaptic protein expression. • Ferrostatin-1 represses P38 MAPK activation and mitigate synaptic proteins deficits and cognitive deficits in rats with KA induced TLE. • SB203580 improve cognitive function in rats with KA induced TLE. • P38 MAPK activation mediates synaptic proteins deficits in rats with KA induced TLE. [ABSTRACT FROM AUTHOR]

Highlights: [•] A bone morphogenetic proteins homologue of Schistosoma japonicum was cloned and characterized. [•] SjBMP protein as well as SmBMP is much longer than the homologues from other organisms in the N-terminus. [•] SjBMP does not contain the signal peptide sequences. [•] BMP signaling may be involved in the oviposition behavior of S. japonicum. [Copyright &y& Elsevier]

Background: Insufflation with standard cold-dry CO2 during laparoscopic surgery has been shown to predispose patients to hypothermia and peritoneal injury. This study aimed to compare the effect of prolonged cold-dry CO2 insufflation with heated-humidified CO2 insufflation (3–5 h) on hypothermia, peritoneal damage, and intra-abdominal adhesion formation in a rat model. Materials and methods: A total of 160 Wistar rats were randomized to undergo no insufflation or insufflation with cold-dry CO2 (21°C, <1% relative humidity) or heated-humidified CO2 (37°C, 95% relative humidity) for 3, 4, or 5 h. Core body temperature was measured via rectum before and during insufflations. Peritoneal samples were taken at 6, 24, 48, and 96 h after treatments and analyzed with light microscopy and scanning electron microscopy. Intra-abdominal adhesions were evaluated 2 weeks later. Results: Core body temperature significantly decreased in the cold-dry group, whereas it was maintained and increased in the heated-humidified group. Scanning electron microscopy and light microscopy studies showed intense peritoneal injury in the cold-dry CO2 group but significantly less damages in the heated-humidified group. Increased intra-abdominal adhesion formation was observed in the cold-dry CO2 group, while no adhesions were found in the rats insufflated with heated-humidified CO2. Conclusions: Heated-humidified CO2 insufflation results in significantly less hypothermia, less peritoneal damage, and decreased adhesion formation as compared with cold-dry CO2 insufflation. Heated-humidified CO2 may be more suitable for insufflation application in prolonged laparoscopic surgery. [Copyright &y& Elsevier]

Abstract: Tumor necrosis factor (TNF)-α is a key pro-inflammatory cytokine, thought to be important in the pathogenesis of pulmonary emphysema. TNF-α overexpression in the lung leads to the phenotypic features of pulmonary emphysema, pulmonary hypertension, and right ventricular hypertrophy in mice bred in Denver, 5240feet/1600m of altitude. This study hypothesized that the altitude could affect the development of pulmonary emphysema as well as pulmonary hypertension. To investigate the effect of the altitude, TNF-α transgenic mice were bred at sea level, Fukuoka, Japan. The pulmonary physiology and histology demonstrated similar development of pulmonary emphysema, compared to the mice bred in Denver. With respect to pulmonary hypertension, right ventricular hypertrophy was attenuated. Interestingly, mortality rate was significant lower in the mice bred at sea level. In contrast with the results in Denver, a significant decrease of vascular endothelial growth factor (VEGF) and its receptors expression was not found. From these data, we consider that the altitude affects development of pulmonary hypertension through the expression of VEGF and its receptors. In contrast, the effect of altitude was not clear regarding the development of pulmonary emphysema. [Copyright &y& Elsevier]

NK-lysins, a type of broad-spectrum antimicrobial peptide (AMP), act as an essential effector of innate defense against microbial attack in higher vertebrates and so in fish. The present study delineates the structural and functional characterization of NK-lysin from yellow catfish (Pelteobagrus fulvidrac) (Pelteobagrus fulvidraco). PfNK-lysin encodes a 153-residue peptide, which displays the hallmark features of other known NK-lysins with the ordered array of six well-conserved cysteine residues and five-exon/four-intron structure. It was found to be ubiquitous in tissues, being detected most abundantly in gill and head kidney. In vivo exposure to stimuli (LPS, PolyI:C, and Edwardsiella ictaluri) induced PfNK-lysin expression in head kidney and spleen. Synthetic PfNK-lysin-derived peptide exhibited in vitro bactericidal potency against both Gram-positive and Gram-negative bacteria, with the highest inhibitory effect on pathogen Edwardsiella ictaluri. Fluorescence microscopy and scanning electron microscopy further confirmed its capacity to cause damage to the bacterial plasma membrane. Taken together, these data suggest that PfNK-lysin might participate in antimicrobial defense of yellow catfish by membrane-disruptive action. • A NK-lysin homologue (PfNK-lysin) was identified and characterized from yellow catfish. • PfNK-lysin could be induced by LPS, PolyI:C, and Edwardsiella ictaluri. • PfNK-lysin derived peptide showed bactericidal potency against both Gram-positive and Gram-negative bacteria. • PfNK-lysin exerted its antibacterial effect through damage of bacterial membranes. [ABSTRACT FROM AUTHOR]

Dental caries is a result of the ecological dysfunction of the polymicrobial community on the tooth surface, which evolves through microbial interactions. In this study, we conducted a thorough analysis of the dental plaque microbiome to comprehend its multi-microbial aetiology. In this study, plaque was collected from healthy tooth surfaces, shallow carious teeth and deep carious teeth, and bacterial composition and abundance were assessed using 16S rRNA high-throughput sequencing. Random forest and LEfSe were used to profile various microorganisms at each stage. Additionally, we developed a molecular ecological network (MEN) based on random matrix theory (RMT) to examine microbial interactions for the first time. Our results reveal that Scardovia wiggsiae , Streptococcus mutans , and Propionibacterium acidifaciens may be associated with initial caries, and Propionibacterium acidifaciens differentiates between shallow and deep caries. As caries progressed, the alpha diversity index declined, indicating a decrease in microbial variety. The network topological indices such as centralization betweenness revealed that the caries network had become more complex, involving more microbial interactions. The shallow network revealed a high negative correlation ratio across nodes, indicating that microbes competed heavily. In contrast, the positive correlation ratio of deep network nodes was high, and microorganisms transitioned from a competitive to a synergistic state. This study suggests that microbial diversity and interactions are critical to caries progression and that future caries research should give greater consideration to the role of microbial interaction factors in caries progression. • Scardovia wiggsiae, Streptococcus mutans, and Propionibacterium acidifaciens may distinguish healthy and superficial caries. • Microbial diversity declines as caries progresses, while the strength of microbial interactions increases. • In deep caries, bacteria may be cooperative, but in shallow carious plaque, there may be significant microbial competition. [ABSTRACT FROM AUTHOR]

A hot spring is a distinctive aquatic environment that provides an excellent system to investigate microorganisms and their function in elemental cycling processes. Previous studies of terrestrial hot springs have been mostly focused on the microbial community, one special phylum or category, or genes involved in a particular metabolic step, while little is known about the overall functional metabolic profiles of microorganisms inhabiting the terrestrial hot springs. Here, we analyzed the microbial community structure and their functional genes based on metagenomic sequencing of six selected hot springs with different temperature and pH conditions. We sequenced a total of 11 samples from six hot springs and constructed 162 metagenome-assembled genomes (MAGs) with completeness above 70% and contamination lower than 10%. Crenarchaeota, Euryarchaeota and Aquificae were found to be the dominant phyla. Functional annotation revealed that bacteria encode versatile carbohydrate-active enzymes (CAZYmes) for the degradation of complex polysaccharides, while archaea tend to assimilate C1 compounds through carbon fixation. Under nitrogen-deficient conditions, there were correspondingly fewer genes involved in nitrogen metabolism, while abundant and diverse set of genes participating in sulfur metabolism, particularly those associated with sulfide oxidation and thiosulfate disproportionation. In summary, archaea and bacteria residing in the hot springs display distinct carbon metabolism fate, while sharing the common energy preference through sulfur metabolism. Overall, this research contributes to a better comprehension of biogeochemistry of terrestrial hot springs. [Display omitted] • Microbial diversity and functional profiles were assessed by constructing 162 MAGs. • Archaea and bacteria differed in carbon bias but had the same energy preference. • Archaea fixed carbon while bacteria degraded complex polysaccharides. • Sulfur-related genes were diverse and abundant in hot springs. [ABSTRACT FROM AUTHOR]

Wnt signaling plays important roles in a variety of developmental and pathological processes. Here we show that Wntless , the main regulator for Wnt secretion, is involved in the innate immune response of the giant freshwater prawn, Macrobrachium rosenbergii . The full-length cDNA of the prawn Wntless (named MrWntless ) is 2173 bp in length and contains a 1602-bp open reading frame (ORF), which is conceptually translated into a 533-amino acids sequence. MrWntless protein contains a highly conserved Wnt-binding domain which is required for secretion of Wnt ligands, and exhibits 57–67% identity with known Wntless proteins of other animals. MrWntless was found to be expressed in a variety of prawn tissues including heart, gill, muscle, gut, hepatopancreas and ovary. Moreover, MrWntless expression was significantly increased in the hepatopancreas and gill of the prawns challenged by the bacterial pathogen Aeromonas hydrophila and Vibrio parahaemolyticus . Knockdown of MrWntless by RNA interference in prawns led to dramatically decreased MrWntless expression of approximately 70%. Furthermore, the cumulative mortality rate of the prawn injected with MrWntless dsRNA was greatly increased in response to A. hydrophila challenge compared with the control prawns. Taken together, we provide evidence that prawn Wntless is important for their innate immune response against bacterial pathogens. [ABSTRACT FROM AUTHOR]

Methyl farnesoate (MF), the crustacean juvenile hormone (JH), plays critical roles in various physiological processes in crustaceans. The titer of MF is precisely regulated by specific carboxylesterase. Here, we report for the first time that the cloning and expression analysis of a JH esterase-like carboxylesterase from the prawn Macrobrachium rosenbergii (named as MrCXE ). MrCXE contained a 1935-bp open reading frame (ORF) conceptually translated into a 644-amino acids protein. MrCXE protein shared the highest identity (36%) with JH esterase-like carboxylesterase from the swimming crab, Portunus trituberculatus and exhibited the typical motifs of JH esterase-like carboxylesterases. MrCXE was most abundantly expressed in hepatopancreas, the major tissue for MF metabolism. MrCXE was expressed at a low level in gut and was not detected in other tissues. Additionally, MrCXE expression was upregulated in hepatopancreas by eyestalk ablation to increase MF level. Furthermore, the mRNA level of MrCXE was significantly increased in the hepatopancreas when challenged by the bacterial pathogens Aeromonas hydrophila and Vibrio parahaemolyticus . To our knowledge, this is the first report that the JH esterase-like carboxylesterase is involved in the innate immune response of the crustaceans. [ABSTRACT FROM AUTHOR]

Recent research highlights the function of regulatory T cells (Tregs) in white matter integrity in CNS diseases. Approaches that expand the number of Tregs have been utilized to improve stroke recovery. However, it remains unclear if Treg augmentation preserves white matter integrity early after stroke or promotes white matter repair. This study evaluates the effect of Treg augmentation on white matter injury and repair after stroke. Adult male C57/BL6 mice randomly received Treg or splenocyte (2 million, iv) transfer 2 h after transient (60 min) middle cerebral artery occlusion (tMCAO). Immunostaining showed improved white matter recovery after tMCAO in Treg-treated mice compared to mice received splenocytes. In another group of mice, IL-2/IL-2 antibody complexes (IL-2/IL-2Ab) or isotype IgG were administered (i.p) for 3 consecutive days starting 6 h after tMCAO, and repeated on day 10, 20 and 30. The IL-2/IL-2Ab treatment boosted the number of Tregs in blood and spleen and increased Treg infiltration into the ischemic brain. Longitudinal in vivo and ex vivo diffusion tensor imaging analysis revealed an increase in fractional anisotropy 28d and 35d, but not 14d, after stroke in IL-2/IL-2Ab-treated mice compared to isotype-treated mice, suggesting a delayed improvement in white matter integrity. IL-2/IL-2Ab also improved sensorimotor functions (rotarod test and adhesive removal test) 35d after stroke. There were correlations between white matter integrity and behavior performance. Immunostaining confirmed the beneficial effects of IL-2/IL-2Ab on white matter structures 35d after tMCAO. IL-2/IL-2Ab treatment starting as late as 5d after stroke still improved white matter integrity 21d after tMCAO, suggesting long-term salutary effects of Tregs on the late-stage tissue repair. We also found that IL-2/IL-2Ab treatment reduced the number of dead/dying OPCs and oligodendrocytes in the brain 3d after tMCAO. To confirm the direct effect of Tregs on remyelination, Tregs were cocultured with lysophosphatidyl choline (LPC)-treated organotypic cerebella. LPC exposure for 17 h induced demyelination in organotypic cultures, followed by gradual spontaneous remyelination upon removal of LPC. Co-culture with Tregs accelerated remyelination in organotypic cultures 7d after LPC. In conclusion, Boosting the number of Tregs protects oligodendrocyte lineage cells early after stroke and promotes long-term white matter repair and functional recovery. IL-2/IL-2Ab represents a feasible approach of Treg expansion for stroke treatment. • Regulatory T cells (Tregs) promote white matter repair after stroke. • Tregs provide protection to OPCs and oligodendrocytes early after stroke. • Boosting the number of Tregs improves long-term functional recovery after stroke. [ABSTRACT FROM AUTHOR]

In the paper, the novel TiO 2 nanoshell arrays coated with Au nanoparticles (NPs) were prepared by a simple and effective fabrication method with thermal decomposing polymer particles. Surface structure and composition of these arrays were evaluated by Scanning Electron Microscope (SEM), Energy Dispersive Spectrometer (EDS), and X-ray photoelectron spectroscopy (XPS). The results indicated that TiO 2 nanoshell coated with Au NPs was changed into Au@TiO 2 composite NPs with the rise of annealing temperature. These novel nanostructures have the potential applications in some research fields, such as photocatalysis, single molecule detection, and novel optoelectronic devices. [ABSTRACT FROM AUTHOR]

Abstract: Oxidative stress plays a critical role in the development of pulmonary fibrosis. However, the effects of treatment with anti-oxidant agents against pulmonary fibrosis have not yet been thoroughly investigated. In this study, the effect of MCI-186, a novel free radical scavenger, on bleomycin-induced pulmonary fibrosis was investigated. Bleomycin (0.05units/mouse) was administered intratracheally into C57Bl/6 mice. MCI-186 was given to bleomycin-treated mice intraperitoneally from (i) day −3 to day 7, or from (ii) day 10 to day 28 after bleomycin administration in successive days. At 28 days after bleomycin administration, pulmonary fibrosis was then assessed by lung histology and hydroxyproline. MCI-186 inhibited H2O2-induced DNA damage in bronchial epithelium in vitro. MCI-186 decreased the lipid peroxide content, a marker for DNA damage, in the lung and reduced 8-OHdG positive cells in the lung in vivo. During the early period (day −3 to day 7) administration, MCI-186 partially attenuated bleomycin-induced pulmonary fibrosis. However, during the late period (day 10 to day 28) MCI-186 exacerbated pulmonary fibrosis, based on the histology and hydroxyproline content. In this condition, MCI-186 in the late period decreased the number of apoptosis cells induced by bleomycin, and therefore it might contribute to the deterioration of pulmonary fibrosis. These data indicate that MCI-186, radical scavenger, has a biphasic effect on bleomycin-induced pulmonary fibrosis in mice. Careful attention should be paid before clinical application of new remedies for pulmonary fibrosis. [Copyright &y& Elsevier]

Abstract: Matrix metalloproteinases (MMPs) expression plays a critical role in extracellular matrix deposition. Although several pieces of evidence have so far indicated that gelatinase contributes to the development of pulmonary fibrosis, the role of collagenase remains uncertain. In this study, we attempted to determine the role of collagenase using a bleomycin-induced pulmonary fibrosis model. Bleomycin was instilled into mice intratracheally. Bronchoalveolar lavage fluid (BAL) specimens were analyzed for gelatin and casein zymography, as well as by immunoblotting. The histology of the lungs and hydroxyproline contents were also assessed. MMPs inhibitor, CGS27023A, was simultaneously orally administered. Collagenases were induced in BAL fluids after bleomycin administration based on the data of zymography and immunohistochemistry. The co-administration of MMPs inhibitor, CGS27023A, with bleomycin resulted in worsening pulmonary fibrosis with inhibition of collagenase. The worsening of pulmonary fibrosis was mainly induced by CGS27023A administration in the late phase of bleomycin-induced pulmonary fibrosis development, but not in the early phase. The present data indicated that collagenase plays an anti-fibrotic role in the bleomycin-induced pulmonary fibrosis model. Collagenase has a greater effect on fibrosis phase than inflammatory phase in the bleomycin-induced pulmonary fibrosis in the mice. [Copyright &y& Elsevier]

Abstract: Antibiotics can have a biological effect apart from their anti-bacterial effect. We hypothesized that doxycycline could attenuate acute lung injury through its biological effect. Lipopolysaccharide or doxycycline-resistant Streptococcus pneumoniae was administered intratracheally into mice with the co-administration of doxycycline. Thereafter, the lung pathology, intraalveolar inflammatory cells, bacterial number, and matrix metalloproteinases were investigated. Matrix metalloproteinases, neutrophil migration, and alveolar destruction were induced by lipopolysaccharide. Doxycycline was thus found to improve all of these symptoms. In addition, an inhibitor of matrix metalloproteinases, CGS27023A, attenuated lipopolysaccharide-induced lung injury. Doxycycline also attenuated the lung injury induced by doxycycline-resistant S. pneumoniae and improved the mortality rate although the bacterial number in the lung did not change. Our data indicated that doxycycline could attenuate acute lung injury through a biological effect that was different from its antibiotic effect. [Copyright &y& Elsevier]

Apolipoprotein M (apoM) is a recently discovered human apolipoprotein predominantly present in high-density lipoprotein (HDL) in plasma, exclusively expressed in liver and in kidney. The function of apoM is yet unknown. The human apoM gene is located in the major histocompatibility complex class III region on chromosome 6. Because many genes located in this region are related to the immune response, we have investigated whether apoM might also be involved in the host inflammatory response. In this study we examined effects of the platelet-activating factor (PAF), tumor necrosis factor (TNF-α), and interleukin-1α (IL-1α) on apoM expression in a hepatoblastoma cell line, HepG2 cells. PAF significantly enhanced the apoM mRNA levels and the secretion of apoM in HepG2 cell cultures. The enhancement of apoM secretion is seen at a low concentration of PAF (2 ng/ml), whereas a high concentration of PAF increases both the apoM mRNA levels and apoM secretion. Neither TNF-α nor IL-1α influenced apoM mRNA level and secretion. Furthermore, Lexipafant, a PAF-receptor (PAF-R) antagonist significantly suppressed the mRNA level and the secretion of apoM in HepG2 cells in a dose-dependent manner. Neither PAF nor Lexipafant influenced the mRNA levels and the secretion of apoA-I, apoB and apoE in HepG2 cells, indicating that the effects of PAF or Lexipafant on the apoM production on hepatic cells are selective for apoM. The cellular mechanism of the effects of PAF or Lexipafant on apoM metabolism requires further investigations. [Copyright &y& Elsevier]

TGFβ-activated kinase 1 (TAK1) is a master regulator that drives multiple cell death and proinflammatory signaling pathways, making it a promising therapeutic target to treat ischemic stroke. However, whether targeting TAK1 could improve stroke outcomes has never been tested in female subjects, hindering its potential translation into clinical use. Here we examined the therapeutic effect of 5Z-7-Oxozeaenol (OZ), a selective TAK1 inhibitor, in ovariectomized female mice after middle cerebral artery occlusion (MCAO). OZ significantly reduced neuronal cell death and axonal injury at the acute stage and mitigated neuroinflammation at the subacute stage after MCAO in ovariectomized female mice. Consistent with RNA sequencing analysis that TAK1 activation contributed to microglia/macrophage-mediated inflammatory responses in the post-stroke brain, inhibition of TAK1 with OZ caused phenotypic shift of microglia/macrophages toward an inflammation-resolving state. Furthermore, microglia/macrophage-specific TAK1 knockout (TAK1 mKO) reproduced OZ's effects, causally confirming the role of TAK1 in determining proinflammatory microglial/macrophage responses in post-stroke females. Post-stroke treatment with OZ for 5 days effectively promoted long-term neurological recovery and the integrity of both gray matter and white matter in female mice. Together, the TAK1 inhibitor OZ elicits long-lasting improvement of stroke outcomes in female mice, at least partially through enhancing beneficial microglial/macrophage responses and inflammation resolution. Given its therapeutic efficacy on both male and female rodents, TAK1 inhibitor is worth further investigation as a valid treatment to ischemic stroke. • RNA-seq predicts TAK1 to contribute to neuroinflammation in post-stroke female mice • TAK1 inhibitor reduces neuronal death and inflammation in post-stroke female mice • TAK1 inhibitor/cKO boosts inflammation-resolving microglia/macrophages in females • TAK1 inhibitor/cKO improves long-term stroke outcomes in ovariectomized female mice [ABSTRACT FROM AUTHOR]